Phagocyte migration and cellular stress induced in liver, lung, and intestine during sleep loss and sleep recovery

Everson, Carol A.; Thalacker, Christa D.; Hogg, Neil

doi:10.1152/ajpregu.90623.2008

Cited by 30 publications

(30 citation statements)

References 71 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In fact, prolonged periods of sleep deprivation are notorious for promoting neutrophil migration to the extravascular spaces of lung and liver, concomitant with the increased cell stress [16] . Nonetheless, these effects were evident after 5-10 days of total sleep deprivation, indicating again that the effects of sleep deprivation depend on the length and the extent of sleep loss applied (that is, total sleep deprivation vs. PSD).…”

Section: Discussionmentioning

confidence: 99%

“…In humans, experimental sleep deprivation reduced circulating lymphocyte numbers [9][10][11] and decreased the antibody response to hepatitis A vaccination [12] . In rodent studies, Everson and colleagues conducted a number of experiments on rats, demonstrating that total sleep deprivation (SD) increases the invasion of opportunistic bacteria in blood [13] , intestine and mesenteric lymph nodes [14] , concomitant with the increased endotoxin concentrations in serum [15] and increased cell stress [16] .…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Immune Outcomes of Paradoxical Sleep Deprivation on Cellular Distribution in Naive and Lipopolysaccharide-Stimulated Mice

Zager

Ruiz

Tufik

et al. 2012

Neuroimmunomodulation

View full text Add to dashboard Cite

Background/Aims: Several lines of evidence indicate that sleep loss imposes significant consequences on the host defense system, including changes in cell number, activity and distribution. However, it is not clear whether cellular alterations after sleep deprivation are caused by redistribution to immune organs or by death of these cells or how the response to a nonspecific immune activator would be affected. Therefore, the aim of this study was to assess the leukocyte distribution after paradoxical sleep deprivation (PSD) in saline- and lipopolysaccharide-treated mice. Methods: Adult inbred mice were paradoxical sleep deprived (72 h), whereas the controls were kept in their home cages. After PSD, both groups received an injection of either saline or lipopolysaccharide (LPS; 1 or 5 µg/animal, intraperitoneally), 2 h prior to the collection of blood, spleen, lymph nodes and peritoneal wash. Isolated cells were then designated to differential leukocyte count (blood) and flow cytometry analysis of immune cell subsets (immune sites). Results: The data revealed that PSD caused a significant reduction of circulating lymphocytes and a general decrease in all cellular subsets of spleen, mainly T and B cells. However, no alteration in response of PSD was found on other immune sites, such as lymph nodes and peritoneum. Of note, immune cell distribution in response to in vivo LPS stimulation remained unchanged after PSD. Conclusions: Our study provided original evidence concerning the immune outcomes of PSD, indicating that cellular decrease caused by PSD is not restricted to circulation, but also to immune sites. Taken together, our results could help shed light on the physiological mechanisms of leukocyte trafficking.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Immune Outcomes of Paradoxical Sleep Deprivation on Cellular Distribution in Naive and Lipopolysaccharide-Stimulated Mice

Zager

Ruiz

Tufik

et al. 2012

Neuroimmunomodulation

View full text Add to dashboard Cite

show abstract

“…To produce chronic sleep restriction, the disk was rotated for 6 s according to a pattern of disk rotations that had reliably produced reduced and highly fragmented sleep under acute conditions (23,26). In these prior studies, the housing platform had been rotated for 6 s each time sleep onset was detected in a rat to be totally deprived of sleep, which reduced and fragmented the sleep of a paired rat housed on the same platform.…”

Section: Animals and Environmental Conditionsmentioning

confidence: 99%

“…83). Already well established is the fact that acutely sustained total sleep deprivation in laboratory rats results in a progressive negative energy balance (2, 20, 28), suppression of major anabolic hormones (21, 24), and immune-related abnormalities (18,19,26,27) that turn lethal after an average of 16 to 21 days (20,53,55,62). However, rats that obtain nearly half-normal sleep amounts during the same time period do not develop severe pathology and do not die (20,53,55,62).…”

mentioning

confidence: 99%

Recurrent restriction of sleep and inadequate recuperation induce both adaptive changes and pathological outcomes

Everson¹,

Szabó

2009

American Journal of Physiology-Regulatory, Integrative and Comp

Self Cite

View full text Add to dashboard Cite

Everson CA, Szabo A. Recurrent restriction of sleep and inadequate recuperation induce both adaptive changes and pathological outcomes. Am J Physiol Regul Integr Comp Physiol 297: R1430-R1440, 2009. First published August 19, 2009 doi:10.1152/ajpregu.00230.2009.-Chronic restriction of a basic biological need induces adaptations to help meet requisites for survival. The adaptations to chronic restriction of sleep are unknown. A single episode of 10 days of partial sleep loss in rats previously was shown to be tolerated and to result in increased food intake and loss of body weight as principal signs. The purpose of the present experiment was to investigate the extent to which adaptation to chronic sleep restriction would ameliorate short-term effects and result in a changed internal phenotype. Rats were studied during 10 wk of multiple periods of restricted and unrestricted sleep to allow adaptive changes to develop. Control rats received the same ambulatory requirements only consolidated into periods that lessened interruptions of their sleep. The results indicate a latent period of relatively stable food and water intake without weight gain, followed by a dynamic phase marked by enormous increases in food and water intake and progressive loss of body weight, without malabsorption of calories. Severe consequences ensued, marked especially by changes to the connective tissues, and became fatal for two individuals. The most striking changes to internal organs in sleep-restricted rats included lengthening of the small intestine, decreased size of adipocytes, and increased incidence of multilocular adipocytes. Major organs accounted for an increased proportion of total body mass. These changes to internal tissues appear adaptive in response to high energy production, decomposition of lipids, and increased need to absorb nutrients, but ultimately insufficient to compensate for inadequate sleep. sleep rebound; adaptation; metabolism; adiposity; connective tissues; visceral organs CHRONIC DEFICIENCIES IN BASIC biological requirements produce disease. This basic principle has been well established for nutrition, hydration, and oxygen. It also is believed to be true for sleep. However, the specific physiological properties and outcomes of chronic sleep deficiency are not well elucidated. Most studies on the effects of inadequate sleep have employed previously well-rested, young, normal human and animal subjects under conditions of acute and short-term sleep loss. As may be expected, early physical signs of deprivation seem nonspecific, while subject complaints and poor cognitive performance are pronounced (e.g., reviewed in Refs. 7, 38, 48, and 52). Recently, findings in humans undergoing sleep restriction prolonged for six nights suggest sleep loss produces risk factors for obesity, diabetes, and hypertension (45, 71), but questions arise about the extent to which outcomes can be extrapolated to conditions of chronic deficiency and actually become realized. Epidemiological studies show strong linkages between sleep los...

show abstract

“…Another study revealed that three times as many sleep-dependent transcriptional changes occur in the liver relative to the brain, thus suggesting that sleep can selectively affect non-neural tissues [120]. Furthermore, no selective brain pathology has been reported in rats, flies or worms that have been sleep deprived until they die, although those animals showed signs of increased oxidative stress [121, 122]. Lastly, DAF-16/FOXO is required in muscle for normal responses to sleep deprivation in worms [123].…”

Section: Molecular Indicators Of Sleep’s Functionsmentioning

confidence: 99%

Unraveling the Evolutionary Determinants of Sleep

2016

View full text Add to dashboard Cite

Summary Despite decades of intense study, the functions of sleep are still shrouded in mystery. The difficulty in understanding these functions can be at least partly attributed to the varied manifestations of sleep in different animals. Daily sleep duration can range from 4–20 hrs among mammals, and sleep can manifest throughout the brain, or it can alternate over time between cerebral hemispheres, depending on the species. Ecological factors are likely to have shaped these and other sleep behaviors during evolution by altering the properties of conserved arousal circuits in the brain. Nonetheless, core functions of sleep are likely to have arisen early and to have persisted to the present day in diverse organisms. This review will discuss the evolutionary forces that may be responsible for phylogenetic differences in sleep and the potential core functions that sleep fulfills.

show abstract

Phagocyte migration and cellular stress induced in liver, lung, and intestine during sleep loss and sleep recovery

Abstract: Everson CA, Thalacker CD, Hogg N. Phagocyte migration and cellular stress induced in liver, lung, and intestine during sleep loss and sleep recovery.

Cited by 30 publications

References 71 publications

Immune Outcomes of Paradoxical Sleep Deprivation on Cellular Distribution in Naive and Lipopolysaccharide-Stimulated Mice

Immune Outcomes of Paradoxical Sleep Deprivation on Cellular Distribution in Naive and Lipopolysaccharide-Stimulated Mice

Recurrent restriction of sleep and inadequate recuperation induce both adaptive changes and pathological outcomes

Unraveling the Evolutionary Determinants of Sleep

Contact Info

Product

Resources

About